Hypernatremia - 12/4/2012

Hypernatremia – though overall not as common
as its sibling, HYPOnatremia, it is still seen fairly frequently. In one study
of critically ill hospitalized patients, hypernatremia (defined as a sodium
level of >145 mmol/L) was present at admission in around 10% of patients,
and developed during the hospitalization in an additional 3%. At resident report, we talked about a case of
an elderly woman afflicted by a UTI, with bacetermia, who presented with a sodium of 172 – a fairly common
situation you’ll see in our fragile and febrile elderly population.

Before I head into my regular question-based format of talking about things - I wanted to make a clear clinical distinction. Dehydration, i.e. a net free water deficit, IS NOT synonymous with volume depletion. Volume depletion speaks to a pathophysiologic phenomenon where extracellular fluid loss leads to impaired tissue perfusion, and has potential for more advanced hemodynamic compromise (shock). Dehydration can occur WITHOUT volume depletion, and vice versa. Similarly, if extensive, dehydration can LEAD to volume depletion, a scenario we sometimes struggle with from a management standpoint.

Anyway...let’s talk
about the following:

·What are
some of the causes of hypernatremia?

·What are
the clinical manifestations, and how do acute and chronic hypernatremia differ?

·How is
hypernatremia appropriately managed?

What are
some of the causes of hypernatremia?

·Hypernatremia represents a body water deficit
in relation to the body’s overall sodium stores. This can result from either
net water loss, or net sodium gain (e.g., from hypertonic fluid). The former is
much more common, as reflected by the case presented today, and that’s what
I’ll focus on.

·Our body’s capability to maintain a normal
sodium level is remarkably attuned – a slight increase in plasma osmolality
stimulates both ADH secretion and thirst, and this combination allows us to
maintain a plasma osmolality within a 1-2% range despite wide variations in
water/salt intake.

·Net water loss
and resultant hypernatremia in elderly patients with acute illnesses is
multifactorial, and Dr. Lief hit on several key points. First of all, elderly
patients with altered cognition have poor access to free water. In one
retrospective study of around 100 patients, nearly 90% lacked access to free
water. Secondly, elderly patients have an impaired ability to concentrate their
urine due to impaired vasculature in the area of the loop of Henle where the
interstitial medullary gradient for free water absorption is generated.
Finally, urine infections themselves also impair urinary concentrating ability.
Taken together, the elderly, demented, bacteria-in-the-bladder ridden patient
is EXTREMELY susceptible to hypernatremia.

What are the
clinical manifestations, and how do acute and chronic hypernatremia differ?

·As in hyponatremia, the clinical manifestations are a direct result from osmotic shifts in the brain and consequent cerebral
dysfunction. In the context of hypernatremia, brain cells are LOSING water and
shrinking, instead of GAINING water and swelling. Also similar to hyponatremia,
the severity of the presentation depends on the rapidity of the change in
plasma sodium and osmolality.

·Acute hypernatremia, which is generally defined
as occurring over the course of <24 hours, occurs from salt
overload as opposed to net water loss. Acute brain shrinking can lead to
vascular rupture and intracranial bleeding…and the manifestations are what you’d
expect in such a scenario…altered cognition, lethargy, seizures…coma.

·Chronic hypernatremia is a different situation.
As in hyponatremia (feel like I’m writing that a lot...),
the brain adapts by shifting non-sodium/potassium active osmoles into cells,
thereby normalizing cellular volume. This leads to less marked clinical
manifestations as compared to the acute version…

How is
hypernatremia appropriately managed?

·The attached review article goes over the management
of hypernatremia succinctly and conceptually. There are really three things to
consider—the total water deficit, the rate at which you want to correct, and
which fluid you intend on using. Some comments:

·Depending on what you read, some favor the
conventional formula of water water deficit = TBW X (Serum Na/140 – 1) and
others don’t. The main gripe is that it most useful with only pure water loss,
but underestimates the water deficit in patients with primarily hypotonic fluid
loss. The review article uses the formulas displayed on Table 2...whichever way you go, you'll get a decent "guess-timate" of how much free water you'll need to replete before getting the sodium to a normal level.

·Regarding the rate of correction – the
consequences of overly rapid correction are less well defined as compared to
hyponatremia, but the theoretical fear is increasing brain volume above normal,
leading to cerebral edema and encephalopathy. Based largely on retrospective
studies in infants, the recommended rate of correction in chronic hyponatremia
is 0.5meQ/L per hour, i.e., 10meQ/L per day. In acute hypernatremia, where cerebral
adaptation has not had enough time to allow brain volume to go back to normal,
the rate of correction can be more rapid, and recommendations are to decrease
the sodium level to normal within 24 hours.

·The fluid you choose really depends on the
clinical context. If there is significant volume depletion, Normal Saline is the first choice. Though it won’t change the plasma sodium
significantly, it will also not worsen it, and stabilizing the patient is the
priority. Otherwise, hypotonic fluids are used, including ½ NS, D5W most
commonly – the more hypotonic the fluid, the less that has to be given. Since
potassium also effects plasma osmolality, any K put into fluids for concurrent
potassium losses must also be taken into account, as depicted in the formula in
Table 2.

Would highly recommend reading the attached
review article, I find it pretty useful…